Alteration of phosphoinositide degradation by cytosolic and membrane-bound phospholipases after forebrain ischemia : Reperfussion in gerbil : Effects of amyloid beta peptide

摘要: The reperfusion of previously ischemic brain is associated with exacerbation cellular injury. Reperfusion occasionally potentates release intracellular enzymes, influx Ca2+, breakdown membrane phospholipids, accumulation amyloid precursor protein or β-(like) proteins, and apolipoprotein E. In this study, the effect injury on activity cerebral cortex enzymes acting phosphatidyl [3H] inositol (PI) [l4C-arachidonoyl] PI was investigated. Moreover β25–35 degradation by phospholipase(s) normoxic subjected to ichemia-reperfussion determined. Brain ischemia in gerbils (Meriones unguiculatus) induced ligation both common carotid arteries for 5 min then brains were perfused 15 min, 2 h 7 days. Statistically significant activation enzyme(s) involved phosphatidylinositol ischemia-reperfusion observed. Nearly all showed a higher cytosolic phos-pholipase C (PLC) at after ischemia. Concomitantly, enhancement level DAG AA radioactivity short time confirmed active hippocampus. After prolonged days ischemia, membrane-bound forms PI-PLC activated. question arises if alteration membranes phospholipids occurring an episode Aβ enzymes. A neuro-toxic fragment amyloid, 25–35, incubated presence endogenous increased significantly brain. its non-aggregated form, 25–35 activates but aggregated form enzymatic decreased. Thus, exerts similar from reperfussion We conclude that phosphoinositide-phospholipase may contribute pathophysiology delayed neuronal death following specific inhibitor offer therapeutic strategies protect damage triggered Ischemia-reperfusion had no Aβ-evoked alterations synaptic plasma PI-PLC.